Respiratory response to positive inspiratory pressure in the cat: effects of co2 and vagal integrity. Shams, H., and P. Scheid. Institut f[umlaut]ur Physiologie, Ruhr-Universit[umlaut]at Bochum, 44780 Bochum, FRG
APStracts 2:0259A, 1995.
Effects of inspiratory pressure support (IPS) on respiration and activity of inspiratory muscles were tested in 8 anesthetized cats by recording the diaphragmatic electromyogram (EMGD) and respiratory variables at 4 levels of positive inspiratory airway pressure (5,10,15 and 20 cmH2O); onset of IPS was triggered by the inspiratory effort of the animal. When IPS was applied with room air (IPSAir) the respiratory frequency (fR) was reduced compared with spontaneous breathing, and the tidal volume (VT) was significantly increased, which resulted in a fall of arterial PCO2 (PaCO2) at IPS airway pressures (Paw) above 5 cmH2O. Despite this increase in VT, the amplitude of the integrated EMGD (AD) was reduced during IPS at all levels of Paw. When correcting arterial hypocapnia by adding CO2 to the inspirate (IPSCO2), the values of VT at any given Paw were virtually identical with those during IPSAir, but IPS-mediated changes in fR and AD were smaller than those during IPSAir. IPS was also performed after bilateral vagotomy. Vagotomy itself caused VT and AD to increase, and fR to decrease, during spontaneous breathing. In comparison with the corresponding treatment before vagotomy, IPSAir led to a less severe reduction in AD. As a result, VT was more enhanced, and PaCO2 more reduced, after vagotomy than before, both during spontaneous breathing and during IPSAir at all levels of Paw. When, however, isocapnia was restored with IPSCO2 in the vagotomized animal, diaphragmatic activity and fR became very similar to their values during spontaneous breathing, while VT remained elevated as a result of the high positive airway pressure. Our data suggest that in anesthetized cats IPS leads to a diminution of diaphragm activity and that this reduction can be entirely attributed to (i) the hypocapnia, resulting from increased VT, and (ii) the stimulation of pulmonary vagal afferent fibers at positive airway pressure. 

Received 20 September 1994; accepted in final form 6 June 1995.
APS Manuscript Number A981-4.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on  6 July 1995.